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PubMed1993

Primary plasmacytoma of generalized lymph nodes: a long survivor.

Extramedullary plasmacytomas are occasionally seen in the course of multiple myeloma; however, primary plasmacytomas are unusual. Most of the primary plasmacytomas arise in the upper respiratory system, but a plasmacytoma of the lymph nodes is very rare. A case of a 56-year-old female with primary plasmacytoma in the lower mandibular, cervical, axillary, and para-aortic lymph nodes accompanied by IgA Kappa paraproteinemia is described. After ten courses of combination chemotherapy with cyclophosphamide and prednisolone, she obtained complete response. However, 6 years later, she had a relapse of plasmacytoma in the generalized lymph nodes. She received ten treatments of melphalan-prednisolone and again obtained complete response. She has remained well without chemotherapy or recurrent signs for 9 years. It is considered that conventional chemotherapy can be useful for primary plasmacytoma of generalized lymph nodes.

Female↗
PubMedDate not supplied

Plasmacytoma of the eye and orbit.

BACKGROUND: Plasmacytomas of the ocular and adnexal tissue are rare. The variation in their clinical manifestations and potential association with multiple myeloma are not well appreciated. METHODS: We reviewed the clinical features and laboratory data of five cases of plasmacytoma involving the eye and orbit. RESULTS: Plasmacytomas involved the conjunctiva in one case, the orbit in three cases, and the iris in one case. Plasmacytoma was the solitary plasma cell neoplasm in a patient with a conjunctival lesion and another patient with an orbital lesion. Two other patients who developed plasmacytomas of the orbit and iris, respectively, had a known history of multiple myeloma. An orbital plasmacytoma preceded the onset of systemic plasma cell neoplasia in the final patient. CONCLUSION: Plasmacytomas of the eye and orbit are rare. They may or may not be associated with multiple myeloma.

Aged↗
PubMed2001

The promotion of plasmacytoma tumor growth by mesenchymal stroma is antagonized by basic fibroblast growth factor induced activin A.

The mesenchymal stroma has been shown to play a crucial role in the development of multiple myeloma, partly by secretion of interleukin (IL)-6, that serves as a growth factor for myeloma cells. However, it is still unclear which other stromal molecules are involved in the pathogenesis of this disease. We chose, as a model system, a mouse plasmacytoma cell line, which does not respond to IL-6. We found that the formation of mouse plasmacytoma tumors, in an in vivo skin transplantation model, is facilitated by co-injection of these tumor cells along with a mesenchymal stromal cell. The tumor promoting effect of the stroma was reproduced in an in vitro model; stromal cells induced the proliferation of plasmacytoma cells under serum-free conditions. This growth promotion could not be mimicked by a series of cytokines including IL-6 and insulin-like growth factor (IGF)-I implying a role for yet unidentified stromal factors. The in vivo formation of plasmacytoma tumors was reduced following administration of activin A, a cytokine member of the transforming growth factor (TGF)beta superfamily. Furthermore, the in vitro growth promoting effect of the stroma was abrogated by basic fibroblast growth factor (bFGF) which induced a higher stromal expression of activin A. Our results thus show that mesenchymal stroma expresses plasmacytoma growth stimulating activities that overcome the low constitutive level of the plasmacytoma inhibitor, activin A. The expression of activin A is upregulated by bFGF rendering the stroma suppressive for plasmacytoma growth. The balance between the expression of these regulators may contribute to mesenchymal stroma activity and influence the progression of multiple myeloma.

Activins↗
PubMed1982

Molecular cloning of translocations involving chromosome 15 and the immunoglobulin C alpha gene from chromosome 12 in two murine plasmacytomas.

Expression of IgA by plasmacytomas occurs as a result of a DNA rearrangement that brings the variable region gene, VH, a few kilobases 5' to the constant region gene, C alpha. In this study, we show that the allelic nonexpressed C alpha gene also is rearranged in most plasmacytomas. Cloning, restriction mapping, heteroduplex analyses, and sequence analyses of the nonproductively rearrange C alpha genes from two plasmacytomas, M603 and M167, have demonstrated that the nonproductive rearrangement occurs within the alpha switching region, S alpha. In each case, the same DNA sequence has been joined to the 5' side of C alpha and we have termed this DNA "NIRD" (for nonimmunoglobulin rearranged DNA). Southern blotting analyses of genomic DNAs from various IgG-, IgM-, or IgA-producing plasmacytomas suggest that NIRD is rearranged in almost all plasmacytomas. However, NIRD rearranges to the S alpha region only in IgA-producing cells, not in IgM or IgG producers. Cytogenetic evidence has shown that T(12;15) translocations are common in murine plasmacytomas. Immunoglobulin heavy chain genes are located on chromosome 12, and the translocation breakpoint in plasmacytomas occurs near the immunoglobulin genes. NIRD has been mapped to chromosome 15 by Southern blotting analysis of mouse-hamster cell lines, suggesting that the nonproductively rearranged C alpha clones represent the T(12;15) translocations identified cytogenetically. Therefore, we have identified a region of DNA on chromosome 15 that is commonly rearranged in transformed mouse lymphocytes. We speculate on the significance of NIRD in neoplastic transformation of mouse lymphocytes.

Animals↗
PubMed1977

Alteration of cell-surface antigenicity of the mouse plasmacytoma. II. Lack of correlation between synthesis of myeloma protein and alteration of surface antigen.

The correlation between the changes of immunoglobulin synthesis and the surface antigenicity was analyzed by cytotoxicity and quantitative antibody-absorption tests with the cells of immunoglobulin-producing and nonproducing mouse plasmacytoma. IgA-synthesizing BLAB/c plasmacytoma 58-8 and the non-IgA-synthesizing variant of the 58-8 (nonproducer) were killed with rabbit anti-58-8 plasmacytoma cell antiserum, C3H/He anti-BALB/c spleen cell antiserum, and (C57BL/6 X DBA/2)F1 anti-BALB/c plasmacytoma cell MOPC-31C antiserum plus complement, only when the cells were pretreated with pronase. Quantitative absorption tests revealed that the nonproducer, 58-8 had the same amount of plasmacytoma antigen of 58-8 and PC.1 antigen, and a greater amount of H-2d antigen, as did producer 58-8. The same analysis was carried out for the C3H mouse plasmacytoma X5563, which has an M-component of IgG2a. The nonproducer X5563 had a greater amount of H-2k antigen and a smaller amount of the plasmacytoma antigen of X5563 than did the producer X5563. No detectable PC.1 antigen was observed at surfaces of the producer and the nonproducer X5563 cells.

Animals↗
PubMed1997

Testicular and epididymal plasmacytoma: a report of 7 cases, including three that were the initial manifestation of plasma cell myeloma.

We report the cases of six men, 40 to 89 years of age, with testicular (6 cases) or epididymal (1 case) plasmacytoma. Patients presented with a mass in five cases. One tumor was found during evaluation of progressive myeloma. In the final case, the testicular lesion was identified when the patient presented with pathologic fractures. Gross inspection revealed discrete or, less often, ill-defined lesions. Microscopic examination disclosed masses of atypical plasma cells, including binucleated and multinucleated cells and, occasionally, anaplastic cells that obliterated the underlying parenchyma or invaded between seminiferous or epididymal tubules. Immunohistochemical stains on paraffin sections in five cases showed tumor cell expression of monotypic cytoplasmic immunoglobulin. The cells were positive for the leukocyte common antigen (CD45) in three of five cases. All four cases tested were negative for B (CD20) and T (CD3) cell specific antigens and for CD30 and placental alkaline phosphatase. Expression of CD43, CD45RO, and epithelial membrane antigen was found in three, two, and one of four cases respectively. All the patients also had plasma cell neoplasia distant from the testis, identified before (3 cases), concurrent with (3 cases) or after (1 case) the testicular or epididymal plasmacytoma. In one patient a plasmacytoma developed in the contralateral testis three years later; he was alive with plasma cell myeloma 51 months after diagnosis. Another had a plasmacytoma in the contralateral epididymis 8 years later; he also had a nasal cavity plasmacytoma and multiple subcutaneous plasmacytomas, and was alive and well after 26 years. One additional patient was alive with myeloma 6 months later, and four final patients died between 2 months and 3 years after orchiectomy. Three of the four consultation cases in this series were submitted with diagnoses of spermatocytic seminoma, anaplastic seminoma and lymphoma. The diagnosis of plasmacytoma should be borne in mind when examining testicular or paratesticular tumors with a diffuse pattern without glandular differentiation, particularly in men 40 years of age or older.

Adult↗
PubMed2001

Primary lymph node plasmacytomas (plasmacytic lymphomas).

To determine whether primary lymph node plasmacytoma (PLNP) is a distinct entity among other types of plasma cell neoplasia, we analyzed a large series of PLNPs from 2 large lymphoma registries to compare histologic, immunophenotypic, and clinical features of PLNPs, nonnodal extramedullary plasmacytomas, and multiple myeloma. Twenty-five PLNPs (clinical data on 15 cases) were compared with 10 non-lymph node plasmacytomas and 51 cases of multiple myeloma; 36 cases of reactive plasmacytoses were used as controls. The histologic features of PLNP and other extramedullary plasmacytomas were similar. The histologic features of PLNPs were more immature than those of reactive plasmacytoses and less immature than in multiple myeloma. The immunophenotype of PLNPs significantly differed from that of reactive plasmacytoses, other extramedullary plasmacytomas, and multiple myeloma. PLNPs did not progress to multiple myeloma, unlike other extramedullary plasmacytomas, even though survival in PLNPs and other extramedullary plasmacytomas was similar. Our findings suggest that PLNPs may be distinct from other plasma cell dyscrasias.

Adolescent↗
PubMed1992

Functional homology between N-myc and c-myc in murine plasmacytomagenesis: plasmacytoma development in N-myc transgenic mice.

Mouse plasmacytomas induced by pristane oil alone, or in combination with Abelson murine leukemia virus (A-MuLV), regularly carry one of three alternative chromosomal translocations that juxtapose c-myc to immunoglobulin heavy- or light-chain loci. E mu-c-myc transgenic mice develop translocation-free plasmacytomas after induction by pristane oil and/or A-MuLV [Sugiyama, H., Silva, S., Wang, Y., Weber, G., Babonits, M., Rosen, A., Wiener, F. & Klein, G. (1990). Int. J. Cancer, 46, 845-852]. In order to test whether another member of the myc family, N-myc, could play a similar role as c-myc, we treated E mu-N-myc transgenic mice with pristane and helper-free A-MuLV. Of 20 mice that received a single pristane injection followed by A-MuLV, 17 developed plasmacytomas with a mean latency period of 54 +/- 20 days. In a corresponding group that only received a single pristane injection, five out of six transgenic mice developed plasmacytomas with a mean latency period of 142 +/- 32 days. However, after three monthly injections of pristane, all 15 transgenic mice developed plasmacytomas with a mean latency period of 128 +/- 20 days. All plasmacytomas expressed the N-myc transgene, while none of them expressed either c-myc or endogenous N-myc. None of the tumors carried the usual plasmacytoma-associated translocations.

Abelson murine leukemia virus↗
PubMed1987

Multiple intraparenchymal brain plasmacytomas with spontaneous intratumoral hemorrhage.

The case of a patient with two intraparenchymal brain plasmacytomas without cranial or dural attachment and with intratumoral hemorrhage is presented. Computed tomographic (CT) findings are described. Autopsy revealed two discrete intraparenchymal plasmacytomas with intratumoral hemorrhage, one cerebral and one cerebellar. There have been few case reports of brain plasmacytoma without cranial or dural attachment, and this case of multiple such intracranial, intraparenchymal plasmacytomas with hemorrhage is certainly unique. Intratumoral hemorrhage with intracranial plasmacytoma is extraordinarily rare. The literature of intracranial involvement with myeloma and plasmacytoma and the CT appearance of intracranial plasmacytoma are surveyed.

Brain↗
PubMed1992

Plasmacytoma. Treatment results and conversion to myeloma.

Forty-six cases of solitary plasmacytoma were reviewed for response to radiation and progression to multiple myeloma. Cases were classified as solitary plasmacytomas of bone (SPB) (32 cases) or extramedullary plasmacytomas (EP) (14 cases). There was an overall 93% response rate of the tumor to radiation therapy: 62% had a complete response after radiation therapy, whereas 31% had a partial response. Conversion to multiple myeloma was influenced by the type of plasmacytoma; 53% of the patients with SPB converting to myeloma versus 36% of the patients with EP. Time from diagnosis to conversion for patients with SPB showed no evidence of plateau, with conversion continuing to occur even after 17 years. The median survival time for patients after conversion to myeloma was 14.5 months and was not affected by time to conversion. Serum protein level, presence of monoclonal gammopathy, and size of primary lesion were of some prognostic significance in predicting conversion to myeloma. Adjuvant chemotherapy did not affect the incidence of conversion but did appear to delay conversion to myeloma. Seven patients in whom multiple sequential solitary plasmacytomas developed formed a distinct subset, with a median time to a second plasmacytoma of 63 months. In three of these patients, conversion to myeloma occurred subsequently. This study supports the idea of EP having a lower incidence of conversion to myeloma and a different natural history from SPB, with SPB likely to be multiple myeloma in evolution.

Adult↗
PubMed1983

Solitary plasmacytoma.

A retrospective review is presented of nine patients presenting with solitary plasmacytoma. Between 1963 and 1980, these patients were treated with radiation at the Department of Radiation Oncology, University of Louisville. Criteria for admission to this particular study include (1) a solitary focus of plasmacytoma proven by biopsy, (2) normal bone marrow findings (less than 10% plasma cells), and (3) no evidence of disseminated disease. In six patients the primary site was osseous, and in three extramedullary, two of which were located in the nasopharynx and nasal cavity and the third in the stomach. All of the extramedullary plasmacytomas are disease free for periods ranging from 4 to 10 years. Of the six patients with osseous lesions, two developed multiple myeloma in 2 and 3 years, two are NED (No Evidence of Disorder) after 9 years, one died of intercurrent disease, and the remaining patient was NED for 2 years, after which he was lost to follow-up. These results suggest the more favorable prognosis of extramedullary plasmacytoma and support the theory that the solitary plasmacytoma of bone and extramedullary plasmacytoma are distinct disease entities.

Adult↗
PubMed1999

Recurrent non-reciprocal translocations of chromosome 5 in primary T(12;15)-positive BALB/c plasmacytomas.

The majority of inflammation-induced peritoneal BALB/c plasmacytomas (approximately 90%) harbor a balanced T(12;15) chromosomal translocation that deregulates the expression of the proto-oncogene c-myc. Recent evidence suggests that the T(12;15) is an initiating tumorigenic mutation that occurs in early plasmacytoma precursor cells. However, plasmacytomas take a long time to develop (average tumor latency approximately 220 days), which suggests that additional tumor progression events may be required to complete oncogenesis. We hypothesized that such tumor progression events may take the form of secondary chromosomal aberrations that can be detected by spectral karyotyping (SKY). We screened the entire chromosome complement of 18 primary BALB/c plasmacytomas carrying the T(12;15) and found in nine tumors (50% recurrence) secondary cytogenetic aberrations that involved bands D, E and F chromosome (Chr) 5. The Chr 5D-F rearrangements were manifested predominantly as unbalanced translocations with various partner chromosomes. This finding led us to propose the existence of an important plasmacytoma progression locus in the central region of Chr 5, which presumably becomes involved in peritoneal plasmacytoma development by promiscuous chromosomal translocations.

Animals↗
PubMed1983

Tumor-specific tRNA modifications in mouse plasmacytomas and other tumors.

RPC-5 chromatography has been used to analyze the aa-tRNA populations found in normal organs and in various tumors in experimental animals. The most extensively studied animal systems have been mineral-oil-induced mouse plasmacytomas and carcinogen-induced rat hepatomas. Certain aa-tRNA species appear to be tumor-specific, e.g., rat hepatoma phenylalanyl-tRNA1 and plasmacytoma asparaginyl-tRNAs2-4. In addition, one of the tumor-specific peaks of asparaginyl-tRNA can be found in normal livers of animals bearing plasmacytomas at a distant site. Many other significant quantitative and qualitative differences among histologically similar plasmacytomas and between normal tissues and plasmacytomas were observed in the chromatographic patterns of isoaccepting aa-tRNAs for 11 of 20 amino acids. Some of the qualitative differences in chromatographic patterns could be correlated with the tumorous nature of the tissue using computer analysis. The program utilized cluster analysis to compare the RPC-5 patterns of aa-tRNAs from 11 plasmacytomas and two normal tissues for each of the 20 amino acids. The variations in these chromatographic profiles are though to be caused by varying degrees of incomplete synthesis of some of the normally modified nucleosides in tRNAs.

Amino Acid Sequence↗
PubMed1976

Two cases of plasmacytoma in the oral cavity.

Two cases of plasmacytoma in the oral cavity are described. The first case was a plasmacytoma of the palate in a 64-year-old man, which be an oral manifestation of multiple myeloma, with fatal course 17 months after the first examination. The second was a plasmacytoma in a 43-year-old man, manifesting first in the mandible. A review of the recent Japanese dental literature was made: 14 cases were found in the literature exhibiting evidence of plasmacytoma in the oral region. Eight of these patients had oral manifestations of multiple myeloma (IgG myeloma, 3; IgA myeloma, 1; IgD myeloma, 1; B-J myeloma, 1; undetermined, 2). The other six cases were single lesions of plasmacytoma. The ratio of males to females was 1:1. The mandible was more frequently involved than the other oral structures. The site of predilection was the posterior portion of swelling and, less frequently, pain. Surgical treatment was favored in single lesions of plasmacytoma, while in myeloma chemotherapy and a combination of radiotherapy-chemotherapy constituted 75% of treatment.

Adult↗
PubMed2003

Expression of syndecan-1 is a sensitive marker for cutaneous plasmacytoma.

BACKGROUND: Cutaneous plasmacytoma is a well-recognized, yet infrequent, occurrence in multiple myeloma (MM). There are limitations in the morphologic assessment, and as such, the diagnosis presents some difficulty, particularly with the plasmablastic type. METHODS: Pathology reports of 2357 patients with a diagnosis of MM were reviewed. Twenty patients yielded a total of 25 plasmacytomas, 10 of which were analyzed for syndecan-1 immunoreactivity. Bartl grade of bone marrow and cutaneous plasmacytoma was compared and immunoglobulin secretory status of the patients was assessed. RESULTS: The incidence of cutaneous plasmacytoma was found to be 1 in 118 patients with MM. Immunoglobulin secretion was found to be predominantly IgG. There was a trend for the plasmacytoma Bartl grade to be equal to or greater than that of the corresponding bone marrow Bartl grade, suggesting a more aggressive phenotype in the metastatic lesion. CONCLUSION: Syndecan-1 was found to be a sensitive marker for plasmacytomas, independent of cytologic differentiation.

Adult↗
PubMed2001

Early clinical diagnosis of solitary plasmacytoma of the jaws: a case report with a six year follow-up.

The authors reported a case of a solitary mandibular plasmacytoma in a 53-year-old male Caucasian patient. The histological examination of the specimen was positive for a plasmacytoma with anaplastic appearance. Since the patient refused a demolitive surgical treatment, he was treated with a local radiation therapy of 4000 rads over a 20-day period and polychemotherapy with cyclophosphamide, prednisone and melphalan. Six years after starting radiation treatment the patient is free of recurrent primary disease and not affected by multiple localization. In conclusion, the solitary bone plasmacytoma represents an initial stage of the multiple myeloma rather than a distinct clinical pathology. Unfortunately, the diagnosis of the plasmacytoma is only rarely carried out in the early phases of the disease. The importance of the identification of the initial stage without a clear M component, as in the reported case, is self-evident, since the prognosis is related to the mass of plasmacytoma cells that are present at the time of the diagnosis. The purpose of this study is to report an extremely rare case of solitary bone plasmacytoma with a mandibular localization treated with radio- and polychemotherapy.

Antineoplastic Agents, Alkylating↗
PubMed1984

High resolution banding analysis of the involvement of strain BALB/c- and AKR-derived chromosomes No. 15 in plasmacytoma-specific translocations.

Plasmacytomas were induced in (BALB/c X AKR 6;15) X BALB/c backcross mice where one of the BALB/c-derived chromosomes No. 15 was replaced by the AKR(6;15)-derived Robertsonian 6;15 chromosome. (BALB/c X AKR 6;15)F2 mice that were homozygous for Rb 6;15 were mated to BALB/c mice. Plasmacytomas were induced in the progeny by intraperitoneal injection of pristane. The cytogenetic marker permitted the distinctive identification of the two chromosome 15 homologues, including the distal segment involved in the plasmacytoma-specific translocations. 7 of the 10 plasmacytomas contained the typical t(12;15) translocation. The BALB/c-derived 15 chromosome served as the donor of the translocated segment in six of them. In the seventh, the Rb 6;15 chromosome of the AKR strain was the donor. The remaining three tumors contained the same type of intrachromosomal rearrangement. It arose by the pericentric inversion of the Rb 6;15 chromosome, leading to a variant plasmacytoma-associated rcpt (6;15) translocation. Unlike the usual 6;15 variant that arises by a reciprocal exchange between two separate chromosomes, it was generated by an exchange of the distal segments of a single chromosomal element. High resolution banding analysis of the tumors showed that all translocated breakpoints on chromosomes 15, 12, and 6 were identical with the previously described breakpoints characteristic for the typical 12;15 and the variant 6;15 translocation in murine plasmacytomas. It is known that the distal segment of chromosome 15 carries the c-myc oncogene (23). The PC-associated translocations cut across the 5'-exon of c-myc in the majority of the cases (24,26). The severed oncogene is transposed to the Ig-region on the recipient chromosome. Since the BALB/c strain is highly sensitive to PC-induction, we were interested to examine the question whether its chromosome 15 is preferred as the oncogene donor in AKR X BALB/c backcross mice that carry cytogenetically distinguishable 15 chromosomes. Our results show that this is not the case, since the same segment of the AKR-derived chromosome 15 could also serve in the same capacity. This is in contrast with T cell leukemogenesis where we have previously found that the trisomization-associated duplication of chromosome 15 occurred in a highly asymmetrical fashion, depending on the donor strain of No. 15 (9-11).

Animals↗
PubMed1987

Interleukin-HP1, a T cell-derived hybridoma growth factor that supports the in vitro growth of murine plasmacytomas.

We have recently described the purification and NH2-terminal amino acid sequence of a T cell-derived hybridoma growth factor that was provisionally designated interleukin-HP1 (IL-HP1). Here we report that a T cell supernatant containing high titers of this hybridoma growth factor considerably facilitated the establishment of primary cultures of murine plasmacytomas. Most plasmacytoma cell lines derived from such cultures remained permanently dependent on IL-HP1-containing T cell supernatant for both survival and growth in vitro. These cell lines, however, retained their ability to form tumors in irradiated pristane-treated mice. Analytical fractionation of a T cell supernatant rich in IL-HP1 by either gel filtration, isoelectric focusing, or reversed-phase HPLC revealed the existence of only one plasmacytoma growth factor activity that strictly copurified with IL-HP1, strongly suggesting the identity of both factors. This conclusion was further supported by the finding that IL-HP1 purified to homogeneity supported the growth of both B cell hybridomas and plasmacytomas. For half-maximal growth, plasmacytomas, however, required a concentration of IL-HP1 of approximately 30 pM, which is approximately 200 times higher than that required by B cell hybridomas. A clear difference in the specificity of IL-HP1 and B cell stimulatory factor 1 (BSF-1) was demonstrated by the finding that IL-HP1-dependent plasmacytomas did not survive in the presence of BSF-1, whereas helper T cell lines that proliferated in the presence of BSF-1 failed to respond to IL-HP1.

Animals↗